The major long-range goal of this work is to understand how the chick retinal ganglion cell is able to form highly specific connections with appropriate target cells in the optic tectum and how these target cells maintain the ganglion cells trophically. In the long range we should like to know how each of these mechanisms is related to the failure of the retinal ganglion cell axons to regenerate after being severed. The proposal illustrates why the retinal ganglion cell system of the chick is a particularly favorable place to study these issues and why it may be an excellent model system for studying the mechanisms which underlie the failure of regeneration in the central nervous system of higher vertebrates. In this phase of the work we propose to obtain a set of monoclonal antibodies which will bind specifically to the retinal ganglion cell and its various parts. Some candidate monoclonal antibodies for this work have already been obtained and their properties will be studied in more depth. Additional monoclonal antibodies will be obtained by new fusions and screenings. We have established a system that allows long, healthy neurites to grow from chick retinal explants in culture. We will characterize these neurites at a molecular level using the monoclonal antibodies described above. We will determine what factors are necessary to promote the growth and maintenance of these neurites in vitro in the hopes that the in vitro system will provide an assay for factors that are trophic to the retinal ganglion cell in life. The ability of retinal ganglion cell axons in culture to repair themselves after being severed will be examined. Finally, we will continue our studies on monoclonal antibody 224-1A6-A1 found on the surface of all chick neurons as well as heart and muscle but not on liver, gut and other chick tissues. This project bears a relationship to neurological problems arising out of the failure of central tracts to regenerate. By seeking to understand how axon growth is regulated in a single type of CNS neuron we hope to shed light on regeneration failure at a molecular level.